丹参注射液对于急性胰腺炎大鼠血清中NF-κB、TNF-α、IL-6的影响

目的:通过对急性胰腺炎大鼠用丹参注射液时血清中NF-κB、TNF-α、IL-6的影响,从而探讨丹参对急性胰腺炎的治疗的疗效及机理。方法:45只清洁的雄性Wistar大鼠被随机分成为3组:即空白对照组(假手术组)、疾病模型组(AP组)和药物治疗组(丹参组)。在3h、6h、12h时在各组分别取5只大鼠,采用ELISA法测定并比较大鼠血清中的TNF-α、IL-6及采用WESTERN blotting检测胰腺组织NF-κBp65蛋白。结果:将模型组与对照组(假手术组)比较,TNF-α、IL-6的水平增高,胰腺组织NF-κB蛋白也升高(P<0.05);而治疗组(丹参组)上述指标与模型组相比均有下降(P<0.05)。结论:丹参注射液可能通过抑制AP大鼠NF-κB蛋白,从而降低血清中TNF-α、IL-6的浓度水平,控制AP炎症,从而对急性胰腺炎的治疗发挥作用。     

氯胺酮对重症急性胰腺炎肺损伤大鼠NF-κB的影响

目的探讨氯胺酮对重症急性胰腺炎肺损伤大鼠NF-κB的影响。方法60只健康雄性SD大鼠,随机分为对照组,SAP组和氟胺酮干预组（KTM组）,每组20只。应用逆行胰胆管泵注5％牛磺胆酸钠诱导大鼠重症急性胰腺炎。氯胺酮干预组术后腹腔给予4mg／kg氯胺酮。造模后12h检测肺湿重干重比,肺泡灌洗液中蛋白含量和中性粒细胞百分比,并应用原位杂交法检测造模后6h,12h肺组织NF-κBp65mRNA的表达。结果NF-KBp65mRNA在SAP时除肺泡的细胞质内有表达外,出现细胞核内表达,随时间的延长表达逐渐增加,KTM组NF—KBp65mRNA的表达明显下降。结论NF—κB活化与sAP的肺损伤密切相关,氯胺酮可以通过抑制NF-KBp65mRNA的表达起到肺保护作用。     

泻心汤有效组分不同配伍对内毒素肺损伤大鼠NF-κB及IκB表达的影响

目的研究泻心汤有效组分及其配伍对内毒素肺损伤大鼠NF-κB及IκB表达的影响。方法大鼠灌胃给予黄芩总黄酮提取物(TFL)、大黄总游离蒽醌提取物(TFA)、大黄总结合蒽醌提取物(TCA)、TFL与TFA配伍高、低剂量(A高A低)、TFL与TCA配伍(B)及醋酸地塞米松(Dex)4d,末次给药后1h股静脉注射脂多糖(LPS)建立大鼠内毒素肺损伤模型,1、2、4h各组分别处死6只动物,收集肺组织,免疫印记(Western blot)检测核因子κB(NF-κB)、κB抑制因子(IκB)的蛋白表达。结果大黄总游离蒽醌、A高及Dex在1、2、4h均能够明显抑制NF-κB p65的核转位(P<0.01),所有给药组在2、4h均能够明显抑制胞质中的IκBα的降解(P<0.01)。结论泻心汤有效组分及其配伍对内毒素肺损伤大鼠保护作用与抑制NF-κB的核转位及IκB的降解有关。     

氯胺酮对内毒素小鼠肺泡巨噬细胞核因子-κB活化的影响

目的观察不同浓度的氯胺酮对脂多糖(LPS)诱发的小鼠肺泡巨噬细胞核因子(NF)-κB的活化,进一步探讨氯胺酮对急性肺损伤(ALI)/急性呼吸窘迫综合征(ARDS)的应用前景。方法在小鼠肺泡巨噬细胞(PAM)培养液中加入脂多糖(LPS)10μg/ml得到内毒素肺损伤细胞模型。实验分为LPS刺激组(加LPS10μg/ml)、氯胺酮干预组1(同时加入LPS10μg/ml和氯胺酮10μmol/L)、氯胺酮干预组2(同时加入LPS10μg/ml和氯胺酮100μmol/L)、氯胺酮干预组3(同时加入LPS10μg/ml和氯胺酮1000μmol/L)4组。分别于刺激后0.5,1,4,6h留取细胞,用免疫组织化学染色图像分析法检测细胞核中NF-κB活性。结果①LPS+不同浓度的氯胺酮(10,100,1000μmol/L)后,NF-κBp50活性与LPS组相比在1h和4h处有明显的下降(P<0.05),且有剂量依赖性,氯胺酮浓度越大,NF-κBp50活性下降越明显,各组之间差异有统计学意义(P<0.05)。②NF-κBp65活性的检测与NF-κBp50的检测结果相似。结论氯胺酮通过对PAM内NF-κB活化的抑制,可阻止和延缓LPS诱发的ALI的发生,可能有一定的肺保护作用。     

丹参注射液预防大鼠急性胰腺炎及其机制研究

目的观察丹参注射液预防大鼠急性胰腺炎及其对血清肿瘤坏死因子(TNF-α)、白细胞介素(IL-6)、胰腺组织核因子(NF-κB)及氧自由基的影响。方法将60只SD大鼠随机分为6组,分别为假手术组、模型组、乌司他丁组(20 000U/kg)以及丹参注射液低、中、高剂量(0.4、0.8、1.6 m L/kg)组。用5%牛磺胆酸钠(1.0 m L/kg)胰管内注入诱导大鼠急性胰腺炎模型,造模前30 min分别尾iv给予丹参注射液。各组大鼠均于造模6 h后行腹主动脉采血,处死大鼠取胰腺组织标本,检测SD大鼠急性胰腺炎模型血清淀粉酶(AMY)、血浆内毒素(ET)、胰腺病理评分和病死率。并用ELISA法检测血清IL-6、TNF-α浓度的变化,运用免疫组化法检测NF-κB表达水平,同时切取各时间点大鼠胰腺组织,检测丙二醛(MDA)、组织髓过氧化物酶(MPO)及超氧化物歧化酶(SOD)的水平。结果模型组大鼠的血清AMY、血浆ET、病理评分、死亡率、IL-6、TNF-α水平及胰腺组织中NF-κB活性、MDA水平和MPO活性均较假手术组升高(P0.01),而SOD活性则明显降低(P0.05);乌司他丁组和丹参注射液组上述各项指标均较模型组明显改善(P0.05、0.01)。结论丹参注射液可显著降低实验性急性胰腺炎大鼠的IL-6、TNF-α及NF-κB,清除氧自由基,减轻脂质过氧化反应,从而减轻急性胰腺炎病理损害程度,降低急性胰腺炎大鼠的死亡率。     

乌司他丁对急性肺损伤患者血清TNF-α NF-κB的影响

目的研究乌司他丁对急性肺损伤患者血清TNF-α、NF-κB的影响。方法 40例急性肺损伤患者随机分为治疗组和对照组,每组20例,常规积极治疗原发病、进行肺保护性机械通气的基础上,治疗组加用乌司他丁治疗,治疗前后观察血清TNF-α、NF-κB的变化。结果和对照组相比,治疗组患者血清TNF-α和NF-κB的表达水平明显下降,且差异均有统计学意义(P<0.05)。结论在积极治疗原发病、综合治疗基础上应用乌司他丁治疗能抑制急性肺损伤时的炎症通路,对肺损伤具有保护作用。     

胆红素对内毒素肺损伤大鼠中性粒细胞肺浸润的抑制作用

目的:探讨胆红素对急性肺损伤(ALI)的保护作用及其对中性粒细胞肺浸润的抑制作用。方法:用雄性wistar大鼠30只,随机分为正常对照组、ALI模型组、胆红素干预组。检测肺组织肺系数(LI)、支气管肺泡灌洗液(BALF)中白细胞(WBC)计数、中性粒细胞(PMN)百分比。采用免疫组织化学染色测定肺血管内皮细胞NF-κB蛋白的表达。结果:ALI模型组LI,BALF中WBC计数、PMN百分比和肺血管内皮细胞NF-κB核染色阳性细胞百分比均显著高于正常对照组(P<0.01,P<0.001)。胆红素干预组LI,BALF中WBC计数、PMN百分比和NF-κB核染色阳性细胞百分比均显著低于ALI模型组(P<0.01,P<0.05,P<0.001)。结论:胆红素对内毒素导致肺损伤的PMN肺浸润有一定的抑制作用,可能与抑制肺血管内皮细胞NF-κB的表达有关。     

L-精氨酸和氨基胍对内毒素致肺损伤大鼠的影响

目的:观察L-精氨酸和氨基胍对内毒素(LPS)致肺损伤大鼠的影响,探讨其减轻肺损伤的机制.方法:将35只成年大鼠随机平均分为对照组(Con组)、LPS 1组、LPS+L-精氨酸处理组(L-Arg组)、LPS+氨基胍处理组(AG组)、LPS+复合L-精氨酸和氨基胍处理1组(AA 1组).在注射LPS后240分钟开胸采集标本,检测肺组织NF-kB活性;测定血清中NO2-/NO3-浓度和肺血管通透性.另将22只大鼠分为LP5 2组(n=11)和复合L-精氨酸和氨基胍处理2组(AA 2组,n=11),观察大鼠5天内存活率,并对大鼠肺进行病理分析.结果:LPS 1组肺组织NF-κB活性、血中NO2-/NO3-浓度较Con组明显升高(P＜0.05);肺血管通透指数上升(P＜0.05).L-Arg组和AA 1组肺组织NF-κB活性和血中NO2-/NO3-浓度以及肺的通透指数均较LPS 1组明显下降(P＜0.05).但AG组肺组织NF-κB活性较LPS1组变化不明显(P＞0.05).AA 2组与LPS 2组大鼠病死率分别为18.2%和45.5%,两组比较无显著差异(P＞0.05),但AA 2组存活大鼠肺的病理损害程度比LPS2组轻.结论:L-精氨酸能明显抑制LPS诱导大鼠肺NF-κB活性,氨基胍不影响该活性,而复合用药可明显减轻内毒素所致肺损伤的病理改变.     

薄荷油致大鼠肝毒性机制研究

目的考察川楝子致大鼠肝脏损害的毒性机制。方法将大鼠随机分组,薄荷油组口服薄荷油致肝毒性剂量2.4ml/kg,四氯化碳组口服四氯化碳2.5ml/kg,正常组给予同容积溶媒。给药36或48h后,取血,用ELISA法检测血清TNF-α、IL-6含量;取肝组织,用免疫组化法检测肝组织NF-κB、ICAM-1蛋白表达。结果(1)与正常组相比,薄荷油组与四氯化碳组大鼠血清TNF-α、IL-6含量显著升高(P<0.01)。(2)与正常组比较,薄荷油组与四氯化碳组大鼠肝组织NF-κB、ICAM-1蛋白表达显著增强(P<0.01)。结论大鼠一次性口服薄荷油2.4ml/kg,可引起血清TNF-α、IL-6升高,肝组织NF-κB、ICAM-1蛋白表达增强。炎症反应可能是薄荷油致肝毒性的机制之一。     

Apocynin ameliorates endotoxin-induced acute lung injury in rats

Acute lung injury (ALI) is a serious clinical syndrome with a high rate of mortality. In this study, the effects of apocynin, a NADPH-oxidase (NOX) inhibitor on lipopolysaccharide (LPS)-induced ALI in rats were investigated. Male Sprague–Dawley rats were treated with apocynin (10 mg/kg) intraperitoneally (i.p.) 1 h before LPS injection (10 mg/kg, i.p.). The results revealed that apocynin attenuated LPS-induced ALI as it decreased total protein content, lactate dehydrogenase (LDH) activity and the accumulation of the inflammatory cells in the bronchoalveolar lavage fluid (BALF), In addition, apocynin significantly increased superoxide dismutase (SOD) and reduced glutathione (GSH) activities with significant decrease in the lung malondialdehyde (MDA) content as compared to LPS group in lung tissue and decreased pulmonary artery contraction induced by LPS. It also upregulated mRNA expression of inhibitory protein kappaB-alpha (NFκBia) and downregulated mRNA expression of Toll-Like receptor 4 (TLR4) and decreased inflammation observed in lung tissues.Collectively, these results demonstrate the protective effects of apocynin against the LPS-induced ALI in rats through its antioxidant and antiinflammatory effect that may be attributed to the decrease in mRNA expression of TLR4 and increasing that of NFκBia.     

L-硝基精氨酸对大鼠内毒素性肺损伤治疗作用及其机制的研究

目的探讨L-硝基精氨酸（NG—nitro-L—arginine,L—NA）对内毒素性肺损伤大鼠肺表面活性物质（PS）和细胞凋亡的影响,探讨L—NA对肺损伤的保护作用及其机制。方法健康雄性SD大鼠采用舌下静脉注射脂多糖（LPS）复制肺损伤模型,分别于给予LPS 1h和6b后给予0．9％氯化钠溶液（对照纽及LPS组,静脉给药）和L-NA（20mg／kg,静脉给药）（L-NA治疗组）,治疗3h,取肺组织,原位杂交法（ISH）测定肺组织肺表面活性物质蛋白A（SP-A）mRNA;流式细胞术（FCM）检测肺细胞凋亡率;Western blot法检测Caspase-3蛋白的表达;免疫组化法测定Bcl-2和Bax蛋白的表达。结果与对照组比较,大鼠肺损伤后SP-A mRNA表达明显下降（P〈0．01）;细胞凋亡率、Caspase-3和Bax蛋白表达明显升高（P〈0．01）,Bcl-2蛋白表达和Bcl-2／Bax降低（P〈0．01）;肺损伤1h用L—NA治疗3h后,SP-A mRNA阳性细胞表达明显增强（P〈0．05）,细胞凋亡率降低（P〈0．05）;但Caspase-3、Bax、Bcl-2蛋白表达、Bcl-2／Bax与LPS组比较没有明显的变化（P〈0．05）,肺组织病理改变减轻,肺损伤6h用L—NA治疗3h对LPS引起的以上变化没有明显影响。结论肺损伤1h后给予L—NA可减轻内毒素性肺损伤,增强PS表达,减少细胞凋亡是其机制之一。     

银杏叶提取物注射液对脂多糖致大鼠急性肺损伤肺组织的保护作用

目的 观察银杏叶提取物注射液（GBE）对脂多糖（LPS）致大鼠急性肺损伤（ALI）肺组织的保护作用及其可能机制。方法 24只健康雄性Wistar大鼠随机分为对照组、LPS组和GBE组,每组8只。尾静脉注射LPS建立ALI模型,光镜下观察大鼠肺组织形态学改变;检测肺组织中超氧化物歧化酶活性（SOD）和丙二醛（MDA）含量及血清中白细胞介素-6（IL-6）的表达变化。结果 与对照组相比,LPS组肺组织中SOD活性降低、MDA含量增加、血清中IL-6含量增加（P<0.05）;应用GBE后,肺组织SOD活性升高、MDA含量减少、血清中IL-6含量减少（P<0.05）。结论 GBE可有效减轻ALI肺组织的炎症反应,其机制可能与其提高大鼠抗氧化能力、升高血清中IL-6的含量有关。     

Inhibition of inducible nitric oxide synthase attenuates acute endotoxin-induced lung injury in rats

1. In the present study, we investigated the effects of the inducible nitric oxide (iNOS) inhibitors S-methylisothiourea (SMT) and l-N(6)-(1-iminoethyl)-lysine (l-Nil) on endotoxin-induced acute lung injury (ALI), as well as the associated physiological, biomedical and pathological changes, in anaesthetized Sprague-Dawley rats and in rat isolated perfused lungs. 2. Endotoxaemia was induced by an intravenous (i.v.) infusion of lipopolysaccharide (LPS; Escherichia coli 10 mg/kg). Lipopolysaccharide produced systemic hypotension and tachycardia. It also increased the lung weight/bodyweight ratio, lung weight gain, exhaled nitric oxide (NO), the protein concentration in bronchoalveolar lavage and microvascular permeability. 3. Following infusion of LPS, plasma nitrate/nitrite, methyl guanidine, pro-inflammatory cytokines (tumour necrosis factor-alpha and interleukin-1beta) were markedly elevated. Pathological examination revealed severe pulmonary oedema and inflammatory cell infiltration. Pretreatment with SMT (3 mg/kg, i.v.) or l-Nil (3 mg/kg, i.v.) significantly attenuated the LPS-induced changes and ALI. 4. The results suggest that the inflammatory responses and ALI following infusion of LPS are due to the production of NO, free radicals and pro-inflammatory cytokines through the iNOS system. Inhibition of iNOS is effective in mitigating the endotoxaemic changes and lung pathology. Inhibitors of iNOS may be potential therapeutic agents for clinical application in patients with acute respiratory distress syndrome.     

地塞米松对脓毒症大鼠急性肺损伤影响的实验研究

目的 观察急性肺损伤(ALI)肺组织核因子(NF)-κB的活性变化及地塞米松(Dex)的干预作用。方法 采用LPS诱导的急性肺损伤动物模型,将30只SD大鼠随机分为实验组(AU Dex,10只)、模型组(ALI NS,10只)和对照组(NS,10只)三组,实验组在建模成功后腹腔注射地塞米松,模型组在建模成功后腹腔注射相同剂量的生理盐水,对照组仅腹腔注射相同剂量的生理盐水。注药6小时后留取肺组织,用免疫组织化学法结合图像分析仪检测其NF-κBP65、IκB-α蛋白的相对含量,并进行病理学光镜检查。结果ALI大鼠肺组织可见大量出血和炎性细胞浸润,NF-κBP65的蛋白表达明显升高,IκB-α表达显著降低。Dex能明显下调NF-κBP65的蛋白表达,上调IκB-α表达,并能减轻肺组织的损伤程度。结论 NF-κBP65活化在ALI的发生、发展过程中起着重要作用。Dex具有明显的抗炎作用,减少了肺组织损害。     

Effects of sivelestat treatment on acute lung injury in paraquat-intoxicated rats

Abstract

Lung injury is the main cause of death in acute paraquat (PQ) intoxication. Sivelestat (SV), a neutrophil elastase inhibitor, is effective in reducing inflammation in acute lung injury. The aim of this study was to examine the effect of SV on acute lung injury in PQ-intoxicated rats. Seven-week-old male Sprague-Dawley rats were randomly assigned to four groups: (1) control group (group N; n?=?5); (2) PQ?+?normal saline (group P; n?=?6); (3) normal saline?+?SV (group S; n?=?6) and (4) PQ?+?SV (group PS; n?=?6). SV treatment (intraperitoneally [i.p.], 20?mg/kg) was performed 30 minutes after PQ injection (i.p., 100?mg/kg), and injections were continued every hour for a total of five doses. One hour after the last treatment, blood samples were obtained for analysis of interleukin (IL)-6 and tumor necrosis factor alpha (TNF-α). Lung sections were stained with hematoxylin--eosin for light microscopic analysis. Neutrophil infiltration score of group PS was significantly lower than that of group P (p?<?0.05). But, other scores and total score had no significant differences. IL-6 of group PS did not differ, compared to group P. In addition, there were no differences among the four groups. TNF-α of group PS was reduced, in comparison to the level of group P. SV attenuated neutrophil infiltration in PQ-induced acute lung injury in rats. In addition, systemic inflammation was partially suppressed with SV treatment, suppressing TNF-α production. These results suggest that SV reduces paraquat-induced lung injury, at least partially, by inhibiting neutrophil infiltration and TNF-α secretion.     

外源性ghrelin在大鼠重症急性胰腺炎并肾损伤中的作用

目的：探讨外源性ghrelin在大鼠SAP肾损伤中的作用及机制。方法72只Wistar大鼠随机分为假手术组（SO组,n=24）、重症急性胰腺炎模型组（SAP组,n=24）和ghrelin干预组（G组,n=24）。 SAP组、G组均用3.5%牛磺胆酸钠（1ml/kg）按胰胆管逆行注射法制成重症急性胰腺炎模型,G组在制模前30min和制模后3h腹腔内注射ghrelin（10nmol/kg）,SO组、SAP组于相同时间注射等量生理盐水,各实验组大鼠于制模后6h、12h和24h分批取材。光学显微镜下对胰腺和肾脏组织进行病理学评分,全自动生化仪检测血清淀粉酶,酶联免疫吸附法检测血清IL-6、TNF-α、肌酐。结果①SAP组6h、12h、24h血清淀粉酶、肌酐、TNF-α、IL-6,胰腺及肾脏病理评分均较同时间点SO组升高,差异有统计学意义（P<0.05）;②G组6h、12h、24h血清淀粉酶、肌酐、TNF-α、IL-6,胰腺及肾脏病理评分均较同时间点SAP组下降,差异有统计学意义（P<0.05）,但均较同时间点SO组升高,差异有统计学意义（P<0.05）。结论外源性ghrelin通过降低TNF-α、IL-6的水平,减轻炎症反应来减轻SAP的严重程度,同时保护肾脏的生理功能。     

卡托普利治疗重症急性胰腺炎肺损伤的临床研究

目的观察卡托普利治疗重症急性胰腺炎肺损伤的临床疗效。方法选取2014年4月—2016年3月鄂东医疗集团黄石市中心医院收治的重症急性胰腺炎肺损伤患者82例,随机分为对照组和治疗组,每组各41例。对照组给予常规治疗,包括禁饮禁食,补液,维持水、电解质及酸碱平衡,持续胃肠减压,抑制胰酶分泌,防治胰腺继发感染,静脉营养支持。治疗组在对照组基础上静脉滴注卡托普利注射液,50 mg加入到0.9%氯化钠溶液100 m L中,1次/d。两组患者均连续治疗7 d。观察两组的临床疗效,比较两组肺功能指标、白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)。结果治疗后,对照组和治疗组的总有效率分别为80.5%、92.7%,两组比较差异有统计学意义(P0.05)。治疗后,两组血氧分压(Pa O2)和Pa O2/吸入氧浓度(Fi O2)均显著升高,同组治疗前后比较差异有统计学意义(P0.05);且治疗组这些观察指标的升高程度明显优于对照组,两组比较差异具有统计学意义(P0.05)。治疗后,两组IL-6和TNF-α均显著降低,同组治疗前后比较差异有统计学意义(P0.05);且治疗组这些观察指标的下降程度明显优于对照组,两组比较差异具有统计学意义(P0.05)。结论卡托普利治疗重症急性胰腺炎肺损伤具有较好的临床疗效,能改善肺功能,降低炎性因子,安全性较好,具有一定的临床推广应用价值。     

脂多糖致急性肺损伤后Bax/Bcl-2变化

目的观察脂多糖(LPS)致大鼠急性肺损伤(ALI)后大鼠肺泡上皮细胞凋亡情况。方法雄性Wistar大鼠200~250g60只,随机分为两组,分别为对照组和LPS组,每组30只。各组分别注射0·9%氯化钠(NS)或LPS5mg/kg4h后观察呼吸频率,行动脉血气分析;致死后检测肺组织湿/干(W/D)比值,检测肺泡上皮细胞B-细胞淋巴瘤/白血病-2(Bcl-2)、Bcl-2相关X蛋白(Bax)表达。结果LPS组呼吸频率[(108±77)次/min]较对照组[(71±5)次/min]显著增快,且有明显的肺水肿和低氧血症。LPS组Bax蛋白表达阳性细胞率[(6·27±0·84)%]与对照组[(0·48±0·52)%]相比显著增高,Bcl-2蛋白表达阳性细胞率与对照组比较差异无统计学意义。结论促进细胞凋亡的Bax蛋白表达细胞显著增多,使Bax/Bcl-2细胞比例明显增加,可能参与了LPS诱发的ALI的发病机制。     

Effects of alpha 1-acid glycoprotein on acute pancreatitis and acute lung injury in rats

alpha 1-Acid glycoprotein (AAG), a highly negatively charged glycoprotein, well known for its capillary stabilizing effect, was tested in rat models of acute edematous pancreatitis, acute hemorrhagic-necrotizing pancreatitis, and acute respiratory distress syndrome (ARDS). In cerulein-elicited edematous pancreatitis AAG improved histological alterations at 200 mg/kg i.v. and plasma amylase activity at 1800 or 4200 mg/kg i.v. All other parameters (edema, plasma lipase) were not affected in a biologically relevant manner. In glycodeoxycholic acid-induced hemorrhagic-necrotizing pancreatitis AAG was without effect on parameters measured (plasma amylase, plasma lipase activity, histological scores) at 1800 or 4200 mg/kg i.v. At the extremely high dose of 1500 mg/kg i.v. plasma amylase and lipase levels were decreased. In lipopolysaccharide-mediated ARDS, AAG was tested at 50, 200 or 600 mg/kg i.v. AAG, but also the placebo formulation decreased the myeloperoxidase content in the bronchoalveolar lavage fluid. Histological alterations were improved by AAG, however, not by the placebo formulation. Lung water content was not significantly influenced by AAG, whereas Evans blue extravasation was significantly diminished by all three doses of AAG. It is concluded that the edematous pancreatitis is the first in vivo condition with increased extravascular fluid accumulation, in which AAG is not effective. Based on data presented here and literature data, there is evidence for a beneficial effect of AAG in acute lung injury.